Section 3: Patient history: Difference between revisions

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= Clinical reasoning processes =
= Clinical reasoning processes =
<div>In line with the emphasis on clinical reasoning, it is essential that the patient history is used to establish and test hypotheses related to potential adverse events of OMT. It is important to understand that there are very limited diagnostic utility data related to many factors considered here. Therefore, the physical therapist’s aim during the patient history is to make the best judgment on the probability of serious pathology and contraindications to treatment based on available information.</div><div>Many red flags which contraindicate or limit OMT treatment manifest in an obvious way in the patient presentation (Moore et al 2005), such as:</div><div>Contraindications to OMT interventions:</div>
 
*Multi-level nerve root pathology
In line with the emphasis on clinical reasoning, it is essential that the patient history is used to establish and test hypotheses related to potential adverse events of OMT. It is important to understand that there are very limited diagnostic utility data related to many factors considered here. Therefore, the physical therapist’s aim during the patient history is to make the best judgment on the probability of serious pathology and contraindications to treatment based on available information.
*Worsening neurological function
 
*Unremitting, severe, non-mechanical pain
Many red flags which contraindicate or limit OMT treatment manifest in an obvious way in the patient presentation<ref name="Moore 2005">Moore A, Jackson A, Jordan J, et al (2005). Clinical guidelines for the physiotherapy management of whiplash associated disorder. Chartered Society of Physiotherapy, London.</ref>, such as:
*Unremitting night pain (preventing patient from falling asleep)
 
*Relevant recent trauma
Contraindications to OMT interventions:
*Upper motor neuron lesions
 
*Spinal cord damage
*Multi-level nerve root pathology  
*Worsening neurological function  
*Unremitting, severe, non-mechanical pain  
*Unremitting night pain (preventing patient from falling asleep)  
*Relevant recent trauma  
*Upper motor neuron lesions  
*Spinal cord damage  
*And the features detailed in section 3.4
*And the features detailed in section 3.4


Precautions to OMT interventions:
Precautions to OMT interventions:  


*Local infection
*Local infection  
*Inflammatory disease
*Inflammatory disease  
*Active cancer
*Active cancer  
*History of cancer
*History of cancer  
*Long-term steroid use
*Long-term steroid use  
*Osteoporosis
*Osteoporosis  
*Systemically unwell
*Systemically unwell  
*Hypermobility syndromes
*Hypermobility syndromes  
*Connective tissue disease
*Connective tissue disease  
*A first sudden episode before age 18 or after age 55
*A first sudden episode before age 18 or after age 55  
*Cervical anomalies
*Cervical anomalies  
*Throat infections in children
*Throat infections in children  
*Recent manipulation by another health professional
*Recent manipulation by another health professional
<div>However, there are serious conditions which may mimic musculoskeletal dysfunction in the early stages of their pathological progression:</div>
*CAD (e.g. vertebrobasilar insufficiency due to dissection) (Kerry et al, 2008)
*Upper cervical instability (Niere and Torney, 2004), that could compromise the vascular and neurological structures.


A patient experiencing, for example pain from one of these presentations may seek OMT for the relief of the pain (Murphy, 2010; Taylor and Kerry, 2010). It is therefore important that the subtle&nbsp;symptoms of these pathologies are recognised in the patient history. It is also important to recognise risk factors indicating a potential for neuro-vascular pathology. Information is given below to highlight the key components of the patient history in this context.
However, there are serious conditions which may mimic musculoskeletal dysfunction in the early stages of their pathological progression:


= Risk factors =
*CAD (e.g. vertebrobasilar insufficiency due to dissection)<ref name="Kerry 2008">Kerry R, Taylor AJ, Mitchell JM, et al (2008). Cervical arterial dysfunction and manual therapy: A critical literature review to inform professional practice. Manual Therapy 13(4):278-288.</ref>
*Upper cervical instability<ref name="Niere 2004">Niere KR, Torney SK (2004) Clinicians’ perceptions of minor cervical instability. Manual Therapy 9(3):144-150.</ref>, that could compromise the vascular and neurological structures.


==== Cervical arterial dysfunction ====
A patient experiencing, for example pain from one of these presentations may seek OMT for the relief of the pain<ref name="Murphy 2010">Murphy DR (2010). Current understanding of the relationship between cervical manipulation and stroke: what does it mean for the chiropractic profession? Chiropractic and Osteopathy 18:22.</ref><ref name="Taylor 2010">Taylor AJ, Kerry R (2010). A ‘system based’ approach to risk assessment of the cervical spine prior to manual therapy. International Journal of Osteopathic Medicine 13:85-93</ref>. It is therefore important that the subtle&nbsp;symptoms of these pathologies are recognised in the patient history. It is also important to recognise risk factors indicating a potential for neuro-vascular pathology. Information is given below to highlight the key components of the patient history in this context.


The following risk factors are associated with an increased risk of either internal carotid or vertebrobasilar arterial pathology and should be thoroughly assessed during the patient history (Arnold and Bousser, 2005; Kerry et al, 2008):
= Risk factors =


*Past history of trauma to cervical spine / cervical vessels
==== Cervical arterial dysfunction  ====
*History of migraine-type headache
 
*Hypertension
The following risk factors are associated with an increased risk of either internal carotid or vertebrobasilar arterial pathology and should be thoroughly assessed during the patient history<ref name="Arnold 2005">Arnold M, Bousser MG (2005). Carotid and vertebral dissection. Practical Neurology 5:100-109.</ref><ref name="Kerry 2008">Kerry R, Taylor AJ, Mitchell JM, et al (2008). Cervical arterial dysfunction and manual therapy: A critical literature review to inform professional practice. Manual Therapy 13(4):278-288.</ref>:
*Hypercholesterolemia / hyperlipidemia
 
*Cardiac disease, vascular disease, previous cerebrovascular accident or transient ischaemic attack
*Past history of trauma to cervical spine / cervical vessels  
*Diabetes mellitus
*History of migraine-type headache  
*Blood clotting disorders / alterations in blood properties (e.g. hyperhomocysteinemia)
*Hypertension  
*Anticoagulant therapy
*Hypercholesterolemia / hyperlipidemia  
*Long-term use of steroids
*Cardiac disease, vascular disease, previous cerebrovascular accident or transient ischaemic attack  
*History of smoking
*Diabetes mellitus  
*Recent infection
*Blood clotting disorders / alterations in blood properties (e.g. hyperhomocysteinemia)  
*Immediately post partum
*Anticoagulant therapy  
*Trivial head or neck trauma (Haneline and Lewkovich, 2005; Thomas et al, 2011)
*Long-term use of steroids  
*History of smoking  
*Recent infection  
*Immediately post partum  
*Trivial head or neck trauma<ref>Haneline M, Lewkovich G (2004). Identification of internal carotid artery dissection in chiropractic practice. J Can Chiropr Assoc 48(3):206-10.</ref><ref>Thomas LC, Rivett DA, Attia JR, et al (2011). Risk factors and clinical features of craniocervical arterial dissection. Manual Therapy 16(4):351-356.</ref>
*Absence of a plausible mechanical explanation for the patient’s symptoms.
*Absence of a plausible mechanical explanation for the patient’s symptoms.


==== Upper cervical instability ====
==== Upper cervical instability ====


The following risk factors are associated with the potential for bony or ligamentous compromise of the upper cervical spine (Cook et al 2005):
The following risk factors are associated with the potential for bony or ligamentous compromise of the upper cervical spine<ref>Cook C, Brismee JM, Fleming R, et al (2005). Identifiers suggestive of clinical cervical spine instability: a Delphi study of physical therapists. Physical Therapy 85(9):895-906.</ref>:  


*History of trauma (e.g. whiplash, rugby neck injury)
*History of trauma (e.g. whiplash, rugby neck injury)  
*Throat infection
*Throat infection  
*Congenital collagenous compromise (e.g. syndromes: Down’s, Ehlers-Danlos, Grisel, Morquio)
*Congenital collagenous compromise (e.g. syndromes: Down’s, Ehlers-Danlos, Grisel, Morquio)  
*Inflammatory arthritides (e.g. rheumatoid arthritis, ankylosing spondylitis)
*Inflammatory arthritides (e.g. rheumatoid arthritis, ankylosing spondylitis)  
*Recent neck/head/dental surgery.
*Recent neck/head/dental surgery.


= Importance of observation throughout history =
= Importance of observation throughout history =


Signs and symptoms of serious pathology and contraindications / precautions to treatment may manifest during the patient history stage of assessment. This is an opportunity to observe and recognise possible red flag indicators such as gait disturbances, subtle signs of disequilibrium, upper motor neuron signs, cranial nerve dysfunction, and behaviour suggestive of upper cervical instability (e.g. anxiety, supporting head/neck) early in the clinical encounter.
Signs and symptoms of serious pathology and contraindications / precautions to treatment may manifest during the patient history stage of assessment. This is an opportunity to observe and recognise possible red flag indicators such as gait disturbances, subtle signs of disequilibrium, upper motor neuron signs, cranial nerve dysfunction, and behaviour suggestive of upper cervical instability (e.g. anxiety, supporting head/neck) early in the clinical encounter.  


= Differentiation =
= Differentiation =
<div>The following information is provided to assist in the differential diagnosis of musculoskeletal dysfunction from serious pathologies which commonly manifest as musculoskeletal dysfunction (Arnold and Bousser, 2005; Arnold et al, 2006; Kerry et al, 2008; Kerry, 2011):</div>
<div>The following information is provided to assist in the differential diagnosis of musculoskeletal dysfunction from serious pathologies which commonly manifest as musculoskeletal dysfunction<ref>Arnold M, Bousser MG (2005). Carotid and vertebral dissection. Practical Neurology 5:100-109.</ref><ref>Arnold M, Bousser G, Fahrni G, et al (2006). Vertebral Artery Dissection Presenting Findings and Predictors of Outcome. Stroke 37:2499-2503.</ref><ref>Kerry R, Taylor AJ, Mitchell JM, et al (2008). Cervical arterial dysfunction and manual therapy: A critical literature review to inform professional practice. Manual Therapy 13(4):278-288.</ref><ref>Kerry R (2011). Examination of the Upper Cervical Region, Chapter 6, in: Petty NJ (Ed), Neuromusculoskeletal examination and assessment: a handbook for therapists, 4th Edn. Churchill Livingstone, Elsevier, Edinburgh.</ref>:</div><div></div>
<br>
{| width="600" border="1" align="center" cellpadding="1" cellspacing="1"
 
{| width="600" border="1" cellpadding="1" cellspacing="1"
|+ Differential diagnosis
|+ Differential diagnosis
|-
|-
! scope="col" |  
! scope="col" |  
! scope="col" |  
! scope="col" | Internal carotid artery disease
! scope="col" | Vertebrobasilar artery disease
! scope="col" | Vertebrobasilar artery disease
! scope="col" | Upper cervical instability
! scope="col" | Upper cervical instability
|-
|-
! scope="row" | Early presentation
! scope="row" | Early presentation
Mid-upper cervical pain, pain around ear and jaw (carotidynia),<br>head pain (fronto-temporo-parietal);<br>Ptosis;<br>Lower cranial nerve dysfunction (VIII-XII);<br>Acute onset of pain described as "unlike any other”.
| Mid-upper cervical pain, pain around ear and jaw (carotidynia),<br>head pain (fronto-temporo-parietal);<br>Ptosis;<br>Lower cranial nerve dysfunction (VIII-XII);<br>Acute onset of pain described as "unlike any other”.&nbsp;
Mid-upper cervical pain; occipital headache;<br>Acute onset of pain described as "unlike any other”.
| Mid-upper cervical pain; occipital headache;<br>Acute onset of pain described as "unlike any other”.
| Neck and head pain;<br>Feeling of instability;<br>Cervical muscle hyperactivity;<br>Constant support needed for head;<br>Worsening symptoms.
| Neck and head pain;<br>Feeling of instability;<br>Cervical muscle hyperactivity;<br>Constant support needed for head;<br>Worsening symptoms.
|-
|-
Line 88: Line 94:
| Bilateral foot and hand dysthaesia;<br>Feeling of lump in throat;<br>Metallic taste in mouth (VII);<br>Arm and leg weakness;<br>Lack of coordination bilaterally.
| Bilateral foot and hand dysthaesia;<br>Feeling of lump in throat;<br>Metallic taste in mouth (VII);<br>Arm and leg weakness;<br>Lack of coordination bilaterally.
|}
|}
<div></div><div>It is important to consider the above information in the context of the aforementioned risk factors.</div>
= Typical case histories of vascular dysfunction  =
==== Common vertebral artery dissection  ====
'''Case:'''
A 46 year-old female supermarket worker presented to physical therapy with left-sided head (occipital) and neck pain described as “unusual”. She reported a 6 day history of the symptoms following a road traffic accident. The symptoms were progressively worsening. The pain was eased by rest. She reported a history of previous road traffic accidents. Past medical history included hypertension, high cholesterol, and a maternal family history of heart disease and stroke. Cranial nerve tests for VIII, IX, and X were positive and resting blood pressure was 170/110. Two days after assessment, the patient reported an onset of new symptoms including “feels like might be sick”, “throaty” and “feels faint” – especially after performing prescribed neck exercises. Two days after this, she reported a stronger feeling of nausea, loss of balance, swallowing difficulties, speech difficulties and acute loss of memory. Magnetic resonance arteriography revealed an acute hindbrain stroke related to a left vertebral (extra-cranial) artery dissection.


It is important to consider the above information in the context of the aforementioned risk factors.
'''Synopsis:'''


= Typical case histories of vascular dysfunction =
A typical background of vascular risk factors and trauma, together with a classic pain distribution for vertebral arterial somatic pain which was worsening. Positive signs (blood pressure and cranial nerve dysfunction) were suggestive of cervical vascular pathology. Signs of hindbrain ischaemia developed in a typical time period post-trauma.


==== Common vertebral artery dissection ====
==== Vertebral artery with pain as the only clinical feature  ====


'''Case:'''
'''Case:''' A friend presents to a physical therapist with a sore neck and unremitting headache. The individual complains that they “think” their “neck is out”. They ask if they can have their neck manipulated to “put it back in”. The headache has been present for 3-4 days and is getting worse. They note that the pain has been unrelieved by medication (paracetamol) and it appears to be of a mechanical presentation. Without taking a full history and carrying out a physical examination, the physical therapist goes ahead and manipulates the neck. The result was the individual experiencing numbness and paralysis to their left arm and hand.


A 46 year-old female supermarket worker presented to physical therapy with left-sided head (occipital) and neck pain described as “unusual”. She reported a 6 day history of the symptoms following a road traffic accident. The symptoms were progressively worsening. The pain was eased by rest. She reported a history of previous road traffic accidents. Past medical history included hypertension, high cholesterol, and a maternal family history of heart disease and stroke. Cranial nerve tests for VIII, IX, and X were positive and resting blood pressure was 170/110. Two days after assessment, the patient reported an onset of new symptoms including “feels like might be sick”, “throaty” and “feels faint” – especially after performing prescribed neck exercises. Two days after this, she reported a stronger feeling of nausea, loss of balance, swallowing difficulties, speech difficulties and acute loss of memory. Magnetic resonance arteriography revealed an acute hindbrain stroke related to a left vertebral (extra-cranial) artery dissection.
'''Synopsis:''' Investigation post incident identified an intimal tear of the vertebral artery. The key issue in this case is that the presentation was not fully assessed through a detailed history and physical examination. The warning feature from the history of worsening pain, unrelieved by medication, combined with an inadequate physical examination and limited clinical reasoning, all contributed to an unfortunate and probably avoidable outcome.  


'''Synopsis:'''
==== Internal carotid artery dissection  ====


A typical background of vascular risk factors and trauma, together with a classic pain distribution for vertebral arterial somatic pain which was worsening. Positive signs (blood pressure and cranial nerve dysfunction) were suggestive of cervical vascular pathology. Signs of hindbrain ischaemia developed in a typical time period post-trauma.
'''Case:''' A 42 year-old accountant presents to physical therapy with a 5 day history of unilateral neck and jaw pain, as well as temporal headache, following a rear-end motor vehicle collision. There is a movement restriction of the neck and the physical therapist begins to treat with gentle passive joint mobilisations, and advises range of movement exercises. The following day, the patient’s pain is worse, and he has developed an ipsilateral ptosis. The patient’s blood pressure is unusually high.  


==== Vertebral artery with pain as the only clinical feature ====
'''Synopsis:''' On medical investigation, an extra-cranial dissection of the internal carotid artery was found. The patient had underlying risk factors for arterial disease, and the presentation was typical of internal carotid artery dissection, with a key differentiator being the ptosis. A dramatic systemic blood pressure response was a result of this vascular insult.


'''Case:'''
==== Further examples of similar cases can be found in the literature  ====
A friend presents to a physical therapist with a sore neck and unremitting headache. The individual complains that they “think” their “neck is out”. They ask if they can have their neck manipulated to “put it back in”. The headache has been present for 3-4 days and is getting worse. They note that the pain has been unrelieved by medication (paracetamol) and it appears to be of a mechanical presentation. Without taking a full history and carrying out a physical examination, the physical therapist goes ahead and manipulates the neck. The result was the individual experiencing numbness and paralysis to their left arm and hand.


'''Synopsis:'''
<ref>Biousse V, D’Anglejan-Chatillon J, Massiou H (1994). Head pain in non-traumatic artery dissection: a series of 65 patients. Cephalalgia 14:33-36.</ref><ref>Lemesle M, Beuriat P, Becker F, et al (1998). Head pain associated with sixth-nerve palsy: spontaneous dissection of the internal carotid artery. Cephalalgia 18:112-114.</ref><ref>Crum B, Mokri B, Fulgham J (2000). Spinal manifestations of vertebral artery dissection. Neurology 55:302-306.</ref><ref>Zetterling M, Carlstrom C, Konrad P (2000). Internal carotid artery dissection. Acta Neurologica Scandinavica 101:1-7.</ref><ref>Chan CCK, Paine M, O'Day J (2001). Carotid dissection: a common cause of Horner's syndrome. Clinical and Experimental Ophthalmology 29:411-415.</ref><ref>Caplan LR, Biousse V (2004). Cervicocranial arterial dissections. Journal of Neuroophthalmology 24:299-305.</ref><ref>Arnold M, Bousser MG (2005). Carotid and vertebral dissection. Practical Neurology 5:100-109.</ref><ref>Asavasopon S, Jankoski J, Godges JJ (2005). Clinical diagnosis of vertebrobasilar insufficiency: resident’s case problem. Journal of Orthopaedic and Sports Physical Therapy 35:645-650.</ref><ref>Rogalewski A, Evers S (2005). Symptomatic hemicrania continua after internal carotid artery dissection. Headache 45:167-169.</ref><ref>Taylor AJ, Kerry R (2005). Neck pain and headache as a result of internal carotid artery dissection: implications for manual therapists - case report. Manual Therapy 10:73-77</ref><ref>Thanvi B, Munshi SK, Dawson SL, et al (2005). Carotid and vertebral artery dissection syndromes. Postgraduate Medical Journal 81(956):383-8.</ref><ref>Arnold M, Bousser G, Fahrni G, et al (2006). Vertebral Artery Dissection Presenting Findings and Predictors of Outcome. Stroke 37:2499-2503.</ref><ref>Debette S, Leys D (2009). Cervical-artery dissections: predisposing factors, diagnosis, and outcome. Lancet Neurology 8(7):668-78.</ref><ref>Kerry R, Taylor AJ (2009). Cervical arterial dysfunction: knowledge and reasoning for manual physical therapists. Journal of Orthopaedic and Sports Physical Therapy 39(5):378-387.</ref>
Investigation post incident identified an intimal tear of the vertebral artery. The key issue in this case is that the presentation was not fully assessed through a detailed history and physical examination. The warning feature from the history of worsening pain, unrelieved by medication, combined with an inadequate physical examination and limited clinical reasoning, all contributed to an unfortunate and probably avoidable outcome.


==== Internal carotid artery dissection ====


'''Case:'''
A 42 year-old accountant presents to physical therapy with a 5 day history of unilateral neck and jaw pain, as well as temporal headache, following a rear-end motor vehicle collision. There is a movement restriction of the neck and the physical therapist begins to treat with gentle passive joint mobilisations, and advises range of movement exercises. The following day, the patient’s pain is worse, and he has developed an ipsilateral ptosis. The patient’s blood pressure is unusually high.


'''Synopsis:'''
= ''References =
On medical investigation, an extra-cranial dissection of the internal carotid artery was found. The patient had underlying risk factors for arterial disease, and the presentation was typical of internal carotid artery dissection, with a key differentiator being the ptosis. A dramatic systemic blood pressure response was a result of this vascular insult.


==== Further examples of similar cases can be found in the literature ====
<references />


(Biousse et al, 1994; Lemesle et al, 1998; Crum et al, 2000; Zetterling et al, 2000; Chan et al, 2001; Caplan and Biousse, 2004; Arnold and Bousser, 2005; Asavasopon et al, 2005; Rogalewski and Evers, 2005; Taylor and Kerry, 2005; Thanvi et al, 2005; Arnold et al, 2006; Debette and Leys, 2009; Kerry and Taylor, 2009).
''


*''
*[[Section 2: Clinical reasoning as a framework|'''''Click to go back to Section 2: Clinical reasoning as a framework''''']]  
*[[Section 2: Clinical reasoning as a framework|'''''Click to go back to Section 2: Clinical reasoning as a framework''''']]  
*[[Section 4: Planning the physical examination|'''''Click to continue to Section 4: Planning the physical examination''''']]
*[[Section 4: Planning the physical examination|'''''Click to continue to Section 4: Planning the physical examination''''']]

Revision as of 03:54, 21 December 2012

Clinical reasoning processes[edit | edit source]

In line with the emphasis on clinical reasoning, it is essential that the patient history is used to establish and test hypotheses related to potential adverse events of OMT. It is important to understand that there are very limited diagnostic utility data related to many factors considered here. Therefore, the physical therapist’s aim during the patient history is to make the best judgment on the probability of serious pathology and contraindications to treatment based on available information.

Many red flags which contraindicate or limit OMT treatment manifest in an obvious way in the patient presentation[1], such as:

Contraindications to OMT interventions:

  • Multi-level nerve root pathology
  • Worsening neurological function
  • Unremitting, severe, non-mechanical pain
  • Unremitting night pain (preventing patient from falling asleep)
  • Relevant recent trauma
  • Upper motor neuron lesions
  • Spinal cord damage
  • And the features detailed in section 3.4

Precautions to OMT interventions:

  • Local infection
  • Inflammatory disease
  • Active cancer
  • History of cancer
  • Long-term steroid use
  • Osteoporosis
  • Systemically unwell
  • Hypermobility syndromes
  • Connective tissue disease
  • A first sudden episode before age 18 or after age 55
  • Cervical anomalies
  • Throat infections in children
  • Recent manipulation by another health professional

However, there are serious conditions which may mimic musculoskeletal dysfunction in the early stages of their pathological progression:

  • CAD (e.g. vertebrobasilar insufficiency due to dissection)[2]
  • Upper cervical instability[3], that could compromise the vascular and neurological structures.

A patient experiencing, for example pain from one of these presentations may seek OMT for the relief of the pain[4][5]. It is therefore important that the subtle symptoms of these pathologies are recognised in the patient history. It is also important to recognise risk factors indicating a potential for neuro-vascular pathology. Information is given below to highlight the key components of the patient history in this context.

Risk factors[edit | edit source]

Cervical arterial dysfunction[edit | edit source]

The following risk factors are associated with an increased risk of either internal carotid or vertebrobasilar arterial pathology and should be thoroughly assessed during the patient history[6][2]:

  • Past history of trauma to cervical spine / cervical vessels
  • History of migraine-type headache
  • Hypertension
  • Hypercholesterolemia / hyperlipidemia
  • Cardiac disease, vascular disease, previous cerebrovascular accident or transient ischaemic attack
  • Diabetes mellitus
  • Blood clotting disorders / alterations in blood properties (e.g. hyperhomocysteinemia)
  • Anticoagulant therapy
  • Long-term use of steroids
  • History of smoking
  • Recent infection
  • Immediately post partum
  • Trivial head or neck trauma[7][8]
  • Absence of a plausible mechanical explanation for the patient’s symptoms.

Upper cervical instability[edit | edit source]

The following risk factors are associated with the potential for bony or ligamentous compromise of the upper cervical spine[9]:

  • History of trauma (e.g. whiplash, rugby neck injury)
  • Throat infection
  • Congenital collagenous compromise (e.g. syndromes: Down’s, Ehlers-Danlos, Grisel, Morquio)
  • Inflammatory arthritides (e.g. rheumatoid arthritis, ankylosing spondylitis)
  • Recent neck/head/dental surgery.

Importance of observation throughout history[edit | edit source]

Signs and symptoms of serious pathology and contraindications / precautions to treatment may manifest during the patient history stage of assessment. This is an opportunity to observe and recognise possible red flag indicators such as gait disturbances, subtle signs of disequilibrium, upper motor neuron signs, cranial nerve dysfunction, and behaviour suggestive of upper cervical instability (e.g. anxiety, supporting head/neck) early in the clinical encounter.

Differentiation[edit | edit source]

The following information is provided to assist in the differential diagnosis of musculoskeletal dysfunction from serious pathologies which commonly manifest as musculoskeletal dysfunction[10][11][12][13]:
Differential diagnosis
Internal carotid artery disease Vertebrobasilar artery disease Upper cervical instability
Early presentation Mid-upper cervical pain, pain around ear and jaw (carotidynia),
head pain (fronto-temporo-parietal);
Ptosis;
Lower cranial nerve dysfunction (VIII-XII);
Acute onset of pain described as "unlike any other”.  		Mid-upper cervical pain; occipital headache;
Acute onset of pain described as "unlike any other”. 		Neck and head pain;
Feeling of instability;
Cervical muscle hyperactivity;
Constant support needed for head;
Worsening symptoms.
Late presentation Transient retinal dysfunction (scintillating scotoma, amaurosis fugax);
Transient ischaemic attack;
Cerebrovascular accident. 		Hindbrain transient ischaemic attack (dizziness, diplopia, dysarthria, dysphagia, drop attacks, nausea, nystagmus, facial numbness, ataxia, vomiting, hoarseness, loss of short term memory, vagueness, hypotonia/limb weakness [arm or leg], anhidrosis [lack of facial sweating], hearing disturbances, malaise, perioral dysthaesia, photophobia, papillary changes, clumsiness and agitation);
Cranial nerve dysfunction;
Hindbrain stroke (e.g. Wallenberg’s syndrome, locked-in syndrome). 		Bilateral foot and hand dysthaesia;
Feeling of lump in throat;
Metallic taste in mouth (VII);
Arm and leg weakness;
Lack of coordination bilaterally.
It is important to consider the above information in the context of the aforementioned risk factors.

Typical case histories of vascular dysfunction[edit | edit source]

Common vertebral artery dissection[edit | edit source]

Case:

A 46 year-old female supermarket worker presented to physical therapy with left-sided head (occipital) and neck pain described as “unusual”. She reported a 6 day history of the symptoms following a road traffic accident. The symptoms were progressively worsening. The pain was eased by rest. She reported a history of previous road traffic accidents. Past medical history included hypertension, high cholesterol, and a maternal family history of heart disease and stroke. Cranial nerve tests for VIII, IX, and X were positive and resting blood pressure was 170/110. Two days after assessment, the patient reported an onset of new symptoms including “feels like might be sick”, “throaty” and “feels faint” – especially after performing prescribed neck exercises. Two days after this, she reported a stronger feeling of nausea, loss of balance, swallowing difficulties, speech difficulties and acute loss of memory. Magnetic resonance arteriography revealed an acute hindbrain stroke related to a left vertebral (extra-cranial) artery dissection.

Synopsis:

A typical background of vascular risk factors and trauma, together with a classic pain distribution for vertebral arterial somatic pain which was worsening. Positive signs (blood pressure and cranial nerve dysfunction) were suggestive of cervical vascular pathology. Signs of hindbrain ischaemia developed in a typical time period post-trauma.

Vertebral artery with pain as the only clinical feature[edit | edit source]

Case: A friend presents to a physical therapist with a sore neck and unremitting headache. The individual complains that they “think” their “neck is out”. They ask if they can have their neck manipulated to “put it back in”. The headache has been present for 3-4 days and is getting worse. They note that the pain has been unrelieved by medication (paracetamol) and it appears to be of a mechanical presentation. Without taking a full history and carrying out a physical examination, the physical therapist goes ahead and manipulates the neck. The result was the individual experiencing numbness and paralysis to their left arm and hand.

Synopsis: Investigation post incident identified an intimal tear of the vertebral artery. The key issue in this case is that the presentation was not fully assessed through a detailed history and physical examination. The warning feature from the history of worsening pain, unrelieved by medication, combined with an inadequate physical examination and limited clinical reasoning, all contributed to an unfortunate and probably avoidable outcome.

Internal carotid artery dissection[edit | edit source]

Case: A 42 year-old accountant presents to physical therapy with a 5 day history of unilateral neck and jaw pain, as well as temporal headache, following a rear-end motor vehicle collision. There is a movement restriction of the neck and the physical therapist begins to treat with gentle passive joint mobilisations, and advises range of movement exercises. The following day, the patient’s pain is worse, and he has developed an ipsilateral ptosis. The patient’s blood pressure is unusually high.

Synopsis: On medical investigation, an extra-cranial dissection of the internal carotid artery was found. The patient had underlying risk factors for arterial disease, and the presentation was typical of internal carotid artery dissection, with a key differentiator being the ptosis. A dramatic systemic blood pressure response was a result of this vascular insult.

Further examples of similar cases can be found in the literature[edit | edit source]

[14][15][16][17][18][19][20][21][22][23][24][25][26][27]


References[edit | edit source]

  1. ↑ Moore A, Jackson A, Jordan J, et al (2005). Clinical guidelines for the physiotherapy management of whiplash associated disorder. Chartered Society of Physiotherapy, London.
  2. ↑ 2.0 2.1 Kerry R, Taylor AJ, Mitchell JM, et al (2008). Cervical arterial dysfunction and manual therapy: A critical literature review to inform professional practice. Manual Therapy 13(4):278-288.
  3. ↑ Niere KR, Torney SK (2004) Clinicians’ perceptions of minor cervical instability. Manual Therapy 9(3):144-150.
  4. ↑ Murphy DR (2010). Current understanding of the relationship between cervical manipulation and stroke: what does it mean for the chiropractic profession? Chiropractic and Osteopathy 18:22.
  5. ↑ Taylor AJ, Kerry R (2010). A ‘system based’ approach to risk assessment of the cervical spine prior to manual therapy. International Journal of Osteopathic Medicine 13:85-93
  6. ↑ Arnold M, Bousser MG (2005). Carotid and vertebral dissection. Practical Neurology 5:100-109.
  7. ↑ Haneline M, Lewkovich G (2004). Identification of internal carotid artery dissection in chiropractic practice. J Can Chiropr Assoc 48(3):206-10.
  8. ↑ Thomas LC, Rivett DA, Attia JR, et al (2011). Risk factors and clinical features of craniocervical arterial dissection. Manual Therapy 16(4):351-356.
  9. ↑ Cook C, Brismee JM, Fleming R, et al (2005). Identifiers suggestive of clinical cervical spine instability: a Delphi study of physical therapists. Physical Therapy 85(9):895-906.
  10. ↑ Arnold M, Bousser MG (2005). Carotid and vertebral dissection. Practical Neurology 5:100-109.
  11. ↑ Arnold M, Bousser G, Fahrni G, et al (2006). Vertebral Artery Dissection Presenting Findings and Predictors of Outcome. Stroke 37:2499-2503.
  12. ↑ Kerry R, Taylor AJ, Mitchell JM, et al (2008). Cervical arterial dysfunction and manual therapy: A critical literature review to inform professional practice. Manual Therapy 13(4):278-288.
  13. ↑ Kerry R (2011). Examination of the Upper Cervical Region, Chapter 6, in: Petty NJ (Ed), Neuromusculoskeletal examination and assessment: a handbook for therapists, 4th Edn. Churchill Livingstone, Elsevier, Edinburgh.
  14. ↑ Biousse V, D’Anglejan-Chatillon J, Massiou H (1994). Head pain in non-traumatic artery dissection: a series of 65 patients. Cephalalgia 14:33-36.
  15. ↑ Lemesle M, Beuriat P, Becker F, et al (1998). Head pain associated with sixth-nerve palsy: spontaneous dissection of the internal carotid artery. Cephalalgia 18:112-114.
  16. ↑ Crum B, Mokri B, Fulgham J (2000). Spinal manifestations of vertebral artery dissection. Neurology 55:302-306.
  17. ↑ Zetterling M, Carlstrom C, Konrad P (2000). Internal carotid artery dissection. Acta Neurologica Scandinavica 101:1-7.
  18. ↑ Chan CCK, Paine M, O'Day J (2001). Carotid dissection: a common cause of Horner's syndrome. Clinical and Experimental Ophthalmology 29:411-415.
  19. ↑ Caplan LR, Biousse V (2004). Cervicocranial arterial dissections. Journal of Neuroophthalmology 24:299-305.
  20. ↑ Arnold M, Bousser MG (2005). Carotid and vertebral dissection. Practical Neurology 5:100-109.
  21. ↑ Asavasopon S, Jankoski J, Godges JJ (2005). Clinical diagnosis of vertebrobasilar insufficiency: resident’s case problem. Journal of Orthopaedic and Sports Physical Therapy 35:645-650.
  22. ↑ Rogalewski A, Evers S (2005). Symptomatic hemicrania continua after internal carotid artery dissection. Headache 45:167-169.
  23. ↑ Taylor AJ, Kerry R (2005). Neck pain and headache as a result of internal carotid artery dissection: implications for manual therapists - case report. Manual Therapy 10:73-77
  24. ↑ Thanvi B, Munshi SK, Dawson SL, et al (2005). Carotid and vertebral artery dissection syndromes. Postgraduate Medical Journal 81(956):383-8.
  25. ↑ Arnold M, Bousser G, Fahrni G, et al (2006). Vertebral Artery Dissection Presenting Findings and Predictors of Outcome. Stroke 37:2499-2503.
  26. ↑ Debette S, Leys D (2009). Cervical-artery dissections: predisposing factors, diagnosis, and outcome. Lancet Neurology 8(7):668-78.
  27. ↑ Kerry R, Taylor AJ (2009). Cervical arterial dysfunction: knowledge and reasoning for manual physical therapists. Journal of Orthopaedic and Sports Physical Therapy 39(5):378-387.

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