A patient with conventional and follicular variant papillary thyroid microcarcinoma and Eagle's syndrome, Langlais type III, with hyoid bone variation.

AIM: Presenting an extraordinary case of Eagle's syndrome (ES) with the classical and follicular variant of papillary thyroid microcarcinoma (PTmC) and an uncommon stylohyoid ligament calsification, aside from O'Carroll's System. CASE REPORT: A 52-year-old Turkish man with an histopathology of the follicular variant of PTmC (FVPTmC) of his right lobe and conventional PTmC of his left lobe of the thyroid with an adjuvant 100 mCi radioactive iodine (RAI) ablation was admitted. On the routine follow-up of the present case, a lineer structure at the 3rd compartment of neck in his ultrasonography, a styloid ligament calsification in his noncontrast computed tomography (CT), and a left styloid process of the temporal bone of 29 mm in size in his three-dimensional (3D) CT scanning had been revealed. Conclusively, an ES, Langlais Type III with The Calcification Pattern IV, was recognized. DISCUSSION: A noninvasive peroral medical management was administered as a first-line treatment for the neuropathic sequelae of ES and it has provided relief of signs and symptoms without any recurrence to date, for three years and three months. CONCLUSION: To our knowledge, it is an highly extreme and first case of ES in the English literature, recognized in the course of his programmed follow-up of his conventional PTmC and FVPTmC, simultaneously possessing an exceptional stylohyoid ligament calsification, apart from O'Carroll's System, even with an anatomic variation of the hyoid bone. KEY WORDS: Eagle's Syndrome Follicular variant of papillary thyroid microcarcinoma, Hyoid bone variation, Langlais classification, O'Carroll's System, Radioactive iodine, Papillary thyroid microcarcinoma.

Isolated Horner Syndrome From an Elongated Styloid Process (Eagle Syndrome).

Eagle syndrome occurs when an elongated styloid process causes otolaryngological or neurological symptoms or signs. We report a patient who had an isolated asymptomatic Horner syndrome that resulted from a pinned internal carotid artery being dynamically injured by an elongated styloid process during chiropractic neck manipulation. There was no evidence of arterial dissection.

Eagle syndrome revisited: cerebrovascular complications.

Cervical pain caused by the elongation of the styloid process (Eagle syndrome) is well known to otolaryngologists but is rarely considered by vascular surgeons. We report two patients with cerebrovascular symptoms of Eagle syndrome treated in our medical center in the past year. Case 1: an 80-year-old man with acromegaly presented with dizziness and syncope with neck rotation. The patient was noted to have bilateral elongated styloid processes impinging on the internal carotid arteries. After staged resections of the styloid processes through cervical approaches, the symptoms resolved completely. Case 2: a 57-year-old man presented with acute-onset left-sided neck pain radiating to his head immediately after a vigorous neck massage. Hospital course was complicated by a 15-minute transient ischemic attack resulting in aphasia. Angiography revealed bilateral dissections of his internal carotid arteries, with a dissecting aneurysm on the right. Both injuries were immediately adjacent to the bilateral elongated styloid processes. Despite immediate anticoagulation therapy, he experienced aphasia and right hemiparesis associated with an occlusion of his left carotid artery. He underwent emergent catheter thrombectomy and carotid stent placement, with near-complete resolution of his symptoms. Elongated styloid processes characteristic of Eagle syndrome can result in both temporary impingement and permanent injury to the extracranial carotid arteries. Although rare, Eagle syndrome should be considered in the differential diagnosis in patients with cerebrovascular symptoms, especially those induced by positional change.

Spinal-cord compression related to pseudohypoparathyroidism.

We report a 24-year-old male with pseudohypoparathyroidism and a 6-month history of sensory disturbance in both legs which was associated with difficulty in walking. His physical signs included a short stature, a thick neck, short fourth metacarpals and metatarsals, a spastic paraparesis and sphincteric disturbance. His serum electrolytes included low serum calcium and high serum phosphorus levels. CT reconstruction showed compression of the spinal cord in association with ossified ligamentum flavum at the C2-7 and T9-10 levels. These findings were confirmed by MRI scans.

Fractured heterotopic bone in myositis ossificans traumatica.

OBJECTIVE: To discuss the case of a patient with an acute fracture occurring through preexisting, quiescent, posttraumatic heterotopic bone formation of the gastrocnemius muscle. The lesion demonstrated a previously unreported pattern of healing. This case serves to demonstrate an infrequent event with a rare and heretofore unreported sequella. CLINICAL FEATURES: A 54-year-old man with preexisting, mature heterotopic bone within the left gastrocnemius muscle experienced reinjury to the site. The preexisting heterotopic bone was a result of a sporting injury that had occurred 32 years previously. At the time of the new injury, the patient experienced immediate, severe pain. Radiographs demonstrated a nondisplaced oblique fracture through the preexisting heterotopic bone. INTERVENTION AND OUTCOME: The patient was treated with protective wrapping and physiotherapy modalities. Because only the heterotopic bone was involved, the leg was not placed in a cast. Follow-up radiographs obtained 14 weeks later showed callus formation about the fractured site and evidence of union. CONCLUSION: Fractures occurring through mature heterotopic bone formations, such as those seen in myositis ossificans traumatica, are infrequent; callus formation with union of the fractured fragments is an even rarer occurrence.

[An autopsy case of pallido-nigro-luysian atrophy associated with OPLL].

Clinical and neuropathological studies of a case of pallido-nigro-luysian atrophy with thalamic degeneration and ossification of the posterior longitudinal ligament (OPLL) is reported. The patient was a 72-year-old man, suffering from gait disturbance caused by OPLL for about 3 years. The clinical features were characterized by gradual development of disorientation in place, time and person, memory disturbance, vertical gaze palsy and rigidity of extremities. Dysarthria, dysphagia, bradykinesia, masked face and neck dystonia appeared at the advanced stage of his illness. There was no tremor or other involuntary movements. A clinical diagnosis of parkinsonism was suspected. The main neuropathological findings were neuronal loss and gliosis in globus pallidus, substantia nigra, subthalamic nucleus and thalamus. In addition, neuronal loss of the anterior horn of the cervical spinal cord due to compression by OPLL (C4-C7) was recognized. The neuropathological findings of the present case were consistent with systemic degenerative disorder of the nervous system affecting the pallido-nigro-luysian tract. This rare disorder should be considered in the differential diagnosis of parkinsonism in old people.

Ossification of the posterior longitudinal ligaments: a cause of spinal stenosis syndrome.

Spinal Stenosis Syndrome (SSS) causes varying radiculopathies and myelopathies by compressing the spinal cord, rootlets and nerves within the bony canal. An enlarged and ossified posterior longitudinal ligament, a rare cause of the syndrome, can occupy up to 80% of the cervical spinal canal resulting in severe, sometimes permanent myelopathy. The clinical and the radiographic findings are discussed.