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Query: UMLS:C0007859 (neck pain)
 3,931 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of atlanto-axial rotatory fixation (AARF) was presented in a 19-year-old female who developed sudden onset of neck pain and limitation of neck movement after direct carotid angiography for seizure disorder. Neurological examination was negative except for cock-robin posture and mild hypesthesia and hypalgesia in left C2 distribution. Plain films of the cervical spine disclosed abnormal alignment of C1-C2 and possible rotational dislocation. Bilateral selective vertebral angiography showed marked anterior and posterior displacement of left and right vertebral artery, respectively, at the level of C1. On CT metrizamide myelography, there was clockwise rotation of C1 on C2 with locked facet on the left but no evidence of cord compression was found. With diagnosis of AARF, manual reduction under general anesthesia and with fluoroscopic control was first attempted without success. Therefore, the patient underwent open reduction by using high speed air-drill and posterior fusion of C1 to C3 with acryl and wire. Postoperative course was uneventful and the patient went back to work as a computer operator in three months. The etiology of AARF was described by many authors, but in our case, congenital hypogenesis of transverse and alar ligaments plus minor trauma was most suggested. For neurological manifestations of AARF, occipital neuralgia, headache, neck pain, limitation of neck movement and cock-robin posture were reported, but the cock-robin posture was most characteristic and was an important symptom for the early diagnosis. In neuroradiological findings of AARF, plain CT and CT metrizamide myelography are very useful. Because they clearly demonstrate the degree of rotation and interlocking of atlanto-axial joints, and the presence of cord compression.
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PMID:[CT findings and surgical treatment of atlanto-axial rotatory fixation: a case report]. 648 6

We report a rare case of myelopathy caused by compression of the upper cervical cord by the bilateral anomalous vertebral arteries. A 49-year-old man had dragged his right foot for 4 years. He also complained of a tingling sensation in his right arm and occipitalgia. Neurological examination disclosed right hemiparesis, hypalgesia in the right half of the body and hypertonicity of the lower extremities. MRIs showed a flow void area which compressed and distorted the spinal cord bilaterally at the level of the atlas. A vertebral angiogram showed that the bilateral vertebral arteries had pierced the dura matter under the posterior arch of the atlas, turned upward and laterally in the vertebral canal, making vascular loops at the level of the atlas. 3D CT angiography showed the loops convex medially in the anterior part of the vertebral canal. With these findings, we diagnosed the patient as suffering compression of the cervical cord by the bilateral anomalous vertebral arteries. Suboccipital craniectomy and C1 laminectomy were performed. When the dura mater was opened, the dorsolateral aspect of the spinal cord was found to be compressed and indented markedly by the vertebral arteries. To decompress the spinal cord, the vertebral arteries were retracted dorsolaterally by means of Gore-tex tape and anchored to the spinous process of the axis. Postoperatively, his neurological symptoms improved. Postoperative MRIs showed that the spinal cord was decompressed and had recovered its contour. A review of the literature revealed that only 3 such cases as this one have been reported. The clinical features of these rare cases are nonspecific myelopathy and concomitant occipitalgia or neck pain. The main cause of this rare entity seemed to be the compression of the vertebral artery through its course when it enters the vertebral canal between the atlas and the axis.
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PMID:[Cervical myelopathy caused by bilateral vertebral artery compression]. 948 91

The association between systemic hypertension and headache remains controversial and its pathophysiologic basis is uncertain. A rather characteristic early-morning pulsating headache is commonly seen in hypertensive patients, and a recent meta-analysis supports the link between these 2 entities. Epidemiologic evidence has paradoxically suggested a negative association between hypertension and headache. Unpredictable clinical association between severe hypertension and headache indicates that another cranial perfusion-related variable exerts a critical role. Neuroanatomically, head and neck pain primarily involves the ophthalmic division of the trigeminal nerve (V1). A link between systemic hypertension, pulsatile choroidal blood flow (CBF), and intraocular pressure (IOP) has been established. I propose that a trait ocular sympathetic hypofunction permits rapid episodic ocular choroidal overperfusion that stretches the ocular globe in the cohort of hypertensive patients with headache. Rapid distension of the pain-sensitive corneoscleral envelope can stimulate corneoscleral and iridial pain-sensitive V1 nerve endings and generate headache. Ocular tamponade function physiologically limits choroidal overperfusion. A higher basal IOP in some patients with moderate-to-severe hypertension may dampen pulsatile CBF and account for the negative epidemiologic link between sustained systemic hypertension and headache. Besides activation of the baroreceptor reflex, the association of hypalgesia with hypertension probably involves activation of the vasopressin-endorphin adaptive system consequent to mechanical stimulation of V1. The analogy between hypertensive headache and angle-closure glaucoma is rather limited because typical ocular and visual signs and symptoms of angle-closure glaucoma are not seen in hypertension-related headache. Hypertensive crises, including those associated with pheochromocytoma, are not accompanied by attacks of angle-closure glaucoma. Glaucoma is not associated with ocular choroidal congestion, but with reduced pulsatile CBF. The predisposition to develop angle-closure glaucoma is theoretically not associated with ocular autonomic hypofunction and should be conceptually dissociated from this hypothesis. The hypothesis can be evaluated by establishing significant circadian elevations of blood pressure, including nondipping nighttime pattern as well as circadian and periheadache measurements of IOP in patients with attacks of hypertension-related headache.
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PMID:Systemic hypertension, headache, and ocular hemodynamics: a new hypothesis. 1740 87