Cases reported "Whiplash Injuries"

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31/66. Upper cervical trauma in motor vehicle collisions.

    Motor vehicle collisions can cause a variety of injuries in pedestrians and vehicle occupants. Fatal and nonfatal trauma to the upper cervical spine, that is, atlanto-occipital junction, atlas and axis, can be part of this spectrum. Certain distinctive injuries (for example, "hangman's fracture") which occur result from the unique anatomic structure of this area and the various disruptive forces such as extension, distraction (tension), compression (axial loading), shear, and inertia generated during collision. Correlation of autopsy findings or radiological information of these cervical injuries or both with scene investigation can be informative not only in the determination of morbidity and mortality, but also in the assessment of injury mechanisms and improvements in occupant protection.
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32/66. Traumatic retropharyngeal hematoma.

    The development of a retropharyngeal hematoma following a whiplash injury is a rare occurrence. The potential for airway compression necessitates rapid assessment and treatment. An 80-year-old man who had been receiving long-term aspirin therapy sustained a retropharyngeal hematoma following a motor vehicle accident. Management consisted of tracheostomy, neck exploration, and evacuation and drainage of the hematoma. To the best of our knowledge, there are less than 20 citations of traumatic retropharyngeal hematoma in the English literature. Retropharyngeal hematoma has been associated with cervical extension/flexion injuries, anticoagulation therapy, great-vessel trauma, and foreign body ingestion.
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33/66. The perilymph fistula syndrome defined in mild head trauma.

    Neurological and neuro-otological studies were carried out on 102 adults with mild cranio-cervical trauma productive of positional vertigo and perilymph fistula as confirmed by laboratory tests, and by the finding of perilymph fistula at tympanotomy in the surgically managed group. In this patient group, all other neurological and neuro-otological diagnoses were excluded, e.g. epilepsy, cerebral palsy, multiple sclerosis, retardation; and for the neuro-otological group those with a history of ototoxicity, labyrinthitis, Meniere's disease, chronic ear infections, or developmental or familial disorders. Emphasis in this study was on mild trauma: fewer than half of the sample had been rendered unconscious in the injury of record, and a third of the cases were of whiplash type, with no loss of consciousness (LOC) and no remembered headstrike. These concomitant lesions comprise the perilymph fistula syndrome (PLFS) with a unique profile of neurological, perceptual, and cognitive deficits resembling a post-concussion injury. A complete description of the clinical picture is given, including psychological, cognitive and diagnostic tests, and the outcome of bedrest vs. surgical management. PLFS can arise from minor trauma, fistula are frequently bilateral (71/102), a mild sensorineural hearing loss is of variable occurrence (53%), secondary hydrops is not uncommon, and women appear more vulnerable than men for developing the syndrome. As based upon combined laboratory techniques and clinical symptomology, fistula were correctly predicted in 61 of 65 laser-operated ears. The positional vertigo component of PLFS was in all cases managed according to a special physical therapy program utilizing exercises for vestibular symptom habituation. Even when diagnosed late, a good-to-excellent outcome was achieved in 70% of treated patients.
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34/66. Induction of involuntary movements by peripheral trauma: an analogy with causalgia.

    Ten patients are described in whom various involuntary movement disorders developed after trauma that was predominantly or entirely peripheral. The interval between injury and onset of movement disorder ranged from 48 hours to 3 years; the injured and painful part was the area initially affected by involuntary movements, although more widespread involvement subsequently occurred. These clinical features resemble the phenomena experienced by some patients with causalgia and suggest the possibility of common mechanisms.
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35/66. "Whiplash"-injury of the 2nd cervical ganglion and nerve.

    Amongst the many patients with persisting neck pain and headache following cervical injuries are a small number in whom the mechanism is compression of the second cervical nerve root and ganglion. This paper describes the clinical features in 14 patients seen by the author. The main features are unilateral pain in the upper cervical and occipital region, tenderness in the suboccipital region, and diminished sensation in the C2 dermatome. The anatomical basis for this syndrome is discussed and illustrated with dissections from a cadaver.
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36/66. Acute paraparesis secondary to Arnold-Chiari type I malformation and neck hyperflexion.

    A 2-year-old child experienced clinical manifestations of Arnold-Chiari Type I malformation, rare in early childhood, after a mild hyperflexion injury of the neck that resulted in acute paraparesis. Recovery occurred after decompressive laminectomy.
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37/66. mediastinitis after whiplash injury.

    The authors describe a rare complication of whiplash injury. Diffuse mediastinitis resulted from extension of a whiplash-induced retropharyngeal abscess into the thorax. early diagnosis of the cervical infection was masked by the simultaneous presence of infectious mononucleosis. Aggressive surgical management including bilateral thoracotomy was required to resolve the septic course. A review of the literature discusses the pathogenesis of this complication including the route of extension into the mediastinum and supports the use of aggressive surgical therapy to reduce the associated mortality.
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38/66. Studies on ataxia of lumbar origin in cases of vertigo due to whiplash injury.

    We draw the following conclusions from clinical observations on traumatized patients with vertigo and lumbar pain. 1) Hypertonicity of the lumbar soft supporting tissues, and especially the lumbar erector muscles (i.e., over-excitment of the lumbar proprioceptors) is a cause of vertigo due to whiplash injury. Equilibrium tests after fixing the waist with a corset are useful for detecting ataxia of lumbar origin. 2) Over-excitement of the lumbar porpiroceptors and dysfunction of the brain stem and the cerebellum are closely related in bringing about vertigo due to whiplash injury. The lumbar proprioceptors in particular may be important, in close correlation with the cerebellum in producing vertigo of this type. 3) Infiltration of procaine into tender spots in the lumbar soft supporting tissues is helpful in therapy of disequilibrium of the eyes and body and of cerebellar ataxia.
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39/66. Traumatic occlusion of both internal carotid arteries.

    Two cases of bilateral occlusion of the extracranial internal carotid artery after blunt trauma to the head and neck are presented. Sixteen similar cases have been reported in the literature, and at least 150 case reports exist on unilateral blunt trauma of carotid arteries. The 25-day post-traumatic latent interval in one of our cases is the longest to date. The diagnosis of both of our cases was established by directional cw-Dopplersonography, whereas previously the only diagnostic method available in cases with negative CT scan and latent interval was angiography. In the differential diagnosis of craniocerebral or craniocervical trauma, particularly following delay between injury and onset of neurological symptoms, Dopplersonography is a necessary test additional.
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40/66. Whiplash maculopathy.

    Maculopathy in three patients, caused by whiphash injury demonstrated three features that are characteristic of this subtle disturbance of the macula: a history of flexion-extension, head and neck trauma; a history of immediate mild reduction of central visual acuity in one or both eyes; and grayish swelling of the foveal zone accompanied by a small (50 to 100-mu) pit or depression in the fovea. In patients with this disturbance, the retinal opacification and the visual disturbance are transient, but the tiny depression in the retina with its whitish border is permanent.
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