Acta Neurochir (2005) [Suppl] 92: 25–27 6 Springer-Verlag 2005
Printed in Austria
Whiplash injury. TOS and double crush syndrome. Forensic medical aspects
C. Schenardi
Medico Legale, Conegliano, Italy
Summary
In this article the author wants to specify that the whiplash syn- drome is underestimated, even by the specialists. In particular the complications aren’t taken into correct consideration, above all if they concern the brachial plexus, especially regarding the TOS syn- drome and double-crush syndrome. This is a problem also among the experts who have to make an evaluation in the field of insurance.
Keywords: Whiplash injury; TOS; double crush syndrome.
The denomination ‘‘Whiplash Injury’’ (WI) derives from the etiopathogenic description of the sudden sharp whipping movement of the head and neck, pro- duced at the moment of a tra‰c accident, particularly following collisions from behind, head-on or side collisions.
WI is characterised by a collection of symptoms that occur following damage to the neck usually as a result of a sudden strain a¤ecting the discs, muscles, nerves, or tendons of the neck caused by a sudden acceleration or deceleration of the head and neck. The head is vio- lently thrown back, forwards or sideways followed by reflex contraction in the opposite direction. Swelling and inflammation occur due to damage caused by the rapid movement which leads to pressure being placed on the nerves often resulting in the classical symptoms of whiplash. Damage to the bones in the neck rarely occurs [9].
Symptoms following an accident may be present immediately or may develop gradually over hours, days, or weeks after the injury. Pain and sti¤ness is caused by pressure being placed on the nerves as a re- sult of tissue swelling which causes muscle spasms.
Symptoms of injury may include.
Range of lesions seen with whiplash – Single-multiple cranial nerve palsies – Peripheral neuropathy
– Dizziness and otoneurological disorders – Thoracic outlet syndrome (TOS) – Visual disturbances
– Post-traumatic sympathetic dystrophy (PTSD) – Double-Multiple crush syndrome
– Discopathy – Rim lesions – Spinal cord injury
– Retropharyngeal hematoma – Damage to subarachnoid space – Mediastinitis
– TMJ injury
– Hypopharyngeal, tracheal, or esophageal perfora- tion
– Brain injury
– Hypothalamic-pituitary-thyroid axis disorder – Damage to sympathetic nerves
– Menstrual disorders
Most people respond to whiplash treatment and recover in a few months, however a substantial per- centage will have painful symptoms for much longer especially the elderly or those with pre existing neck problems who may develop chronic long-term prob- lems which may never resolve [10].
Persistent symptoms lead to chronic whiplash syn- drome which is defined as presence of symptoms for longer than six months. Most of the controversies over WI are related to arguments about the validity of chronic cases [5].
The evaluation and treatment of chronic cases often are obscure by a shroud of litigation and issues of long term disability. As a result, some investigators have concluded that many people who experience chronic syndrome are ‘‘malingering’’ to obtain the monetary benefits of litigation.
It may be more useful to include chronic whiplash into a group of disorders referred to as functional so- matic syndromes.
It may be an oversimplification to conclude that su¤erers of chronic whiplash syndrome are con- sciously exaggerating their symptoms or malingering.
Moreover, studies demonstrate that symptom persis- tence (or worsening) occurs even when litigation issues have been resolved.
The type and extent of injury varies greatly and diagnosis of whiplash is often one of exclusion.
The e¤ectiveness of seatbelts in preventing neck injury has not yet been determined. Some authors suggest that seatbelts may increase the incidence of a whiplash injury: with the strap over one shoulder, the body rotates during impact [9].
Neck pain occurs in 62% to 100% of whiplash injuries [4] and is the hallmark symptom. The pain can radiate into the occipital, shoulder, or midscapular area. Moreover, anterior neck pain syndromes have been described. Headaches, typically in the sub- occipital region, occur in up to 82% of cases.
Other common complaints include thoracolumbar back pain (35% to 42% of cases) and paresthesia of the upper extremities (45%). A variety of theories have been proposed to explain paresthesia, including tho- racic outlet syndrome, myofascial injuries, stretch in- juries of the brachial plexus, central cord injuries, double-multiple crush syndrome. Dysphagia (7% to 18% of cases), dizziness, vertigo, visual and auditory disturbances, and cognitive impairment have also been reported to occur after whiplash. The pathophysio- logic explanation for these symptoms has thus far eluded investigators.
No characteristic signs are associated with whiplash injuries. About 12% to 20% of patients present overt neurologic signs. Sensory impairment following a par- ticular nerve root distribution of the upper extremities, reduced motor strength of the upper extremities, and diminished reflexes have been described.
Many patients have sensations of tingling and numbness in the hands, particularly of the ulnar two fingers. These symptoms can be attributed to nerve root stretch or compression. More commonly they are
intermittent and aren’t associated with overt neuro- logic signs [1]. The paresthesiae may be due to thoracic outlet syndrome arising from stretch or compression of the lower cords of the brachial plexus as they pass be- tween the scalenus anterior muscle and the scalenus medius muscle, and under the clavicle. That injury can cause a fibrosis of the plexus because of the change- ment of microenvironment of the nerves. Trauma to various parts of the peripheral nervous system is as- sociated with the formation of vasogenic oedema (in the epi-peri- and the endoneurium). Oedema may influence microcirculation in nerves and disturb the normal nutrition of the nerve parenchyma. It may be a stimulating factor for production of connective tissue which eventually might lead to endoneurial scar tissue [11]. Direct physical injury to a peripheral nerve readily increases the perineural permeability in some situations. The increased perineural permeability has an early onset and duration of several weeks. A focal axonal lesion which will result in wallerian degenera- tion upsets the normal bidirectional axonal transport mechanisms and the distal stump will su¤er and initi- ate a series of biochemical events leading to axonal destruction [6]. A severe trauma is enough to cause an irreversible damage to the axons, wallerian degenera- tion will take place distal to the injury. Proliferation of fibroblasts changes in the composition of the matrix and collagen formation may result in endoneurial fib- rosis at the site of the lesion and distal to it. This pro- cedure has a duration of several weeks [3]. This can explain a late beginning of symptoms in a distal region (from the neck) and justify the rejection of the plain- ti¤ ’s request by most medical examiners in their legal medical reports. The double-multiple crush syn- drome (D-MCS) can explain some of these questions [8].
This syndrome occurs when a single nerve is com- pressed (crushed) at two separate levels, proximal and distal; the nerve being irritated at some proximal loca- tion like the thoracic outlet (in the shoulder) or in the neck is su¤ering a peripheral nerve entrapment like carpal tunnel or ulnar entrapment at the elbow:
– Median Cervical radiculopathy and CTS*
– Thoracic outlet and CTS – Pronator syndrome and CTS
– Ulnar Cervical radiculopathy and cubital tunnel syndrome
– Thoracic outlet and cubital tunnel syndrome – Cubital tunnel and Guyon’s canal syndrome
26 C. Schenardi
– Radial Cervical radiculopathy and radial tunnel syndrome
*CTS Carpal tunnel syndrome.
After a WI, patients may su¤er from a double crush syndrome [2]. The symptoms are similar to carpal tunnel pathology and/or thoracic outlet syndrome pathology. Cervical disc disease predisposes patients to carpal tunnel syndrome as well as a cubital tunnel syndrome. Compression in the thoracic outlet or at the level of the cervical disc predisposes the median nerve to compression at the level of the pronator teres and the carpal tunnel. Similarly, thoracic outlet with com- pression of the lower trunk predisposes a patient to compression of the ulnar nerve at the cubital tunnel and in Guyon’s canal [7, 13].
Double crush can be seen post traumatically after a whiplash injury. For instance, a hand specialist may overlook a double crush syndrome originating in the neck. Treatment by surgical release of the carpal tunnel syndrome alone is frequently unsuccessful in the long term because of the unrecognized presence of more proximal compression neuropathy [12].
Also the thoracic outlet syndrome is most often produced by hyperextension neck injuries, especially after side impacts in the case of car accidents. When the neck is hyper-extended in the whiplash injuries, the scalene muscles, which hold the neck in place, are torn, causing blood and other fluids to leak into the brachial plexus injury. This causes scar tissue in the brachial plexus.
TOS involves proximal neurovascular structures, symptoms are often confused whith various distal compression neuropathies or cervical radiculopathies.
Also the imaging studies (RX-MRI-CT ) usually fail to demostrate focal pathology. Electrodiagnostic studies aren’t always enough to prove the damage, especially if the physicians aren’t very experienced.
For all these reasons: the outbreak of the symptoms
could be delayed, symptoms are vague, symptoms are far from the neck, tests usually don’t demonstrate the lesions, the insurance companies deny the link between the symptoms and the accident.
Diagnosis and treatment of whiplash will remain a medical enigma [14] as long as the assessment of the damage is made superficially.
References
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Correspondence: Carlo Schenardi, Medico Legale, Via Gera 46, Conegliano (Tv), Italy. e-mail: schenardi@enline.at
Whiplash injury. TOS and double crush syndrome. Forensic medical aspects 27
