Incomplete Horner's Syndrome Research Articles

Internal Carotid Artery Dissection and Asymmetrical Facial Flushing

A 47-year-old woman presented to her primary care physician (PCP) with severe left-sided headache localized in the retrobulbar and temporal region. The PCP suspected migraine and prescribed a nonsteroidal anti-inflammatory drug. But despite analgesic treatment, her headache continued, and she returned to her PCP 2 weeks later. At this visit, the PCP noticed new anisocoria with a miotic pupil on the left. Emergent magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) of neck and brain revealed no acute or subacute cerebral lesions but a narrowing and semicircular wall hematoma of the left internal carotid artery (ICA) up the petrous segment (Figure 1). The wall hematoma resulted in almost complete occlusion of the arterial lumen. Hereafter, she was transferred to our stroke center, where we confirmed diagnosis of ICA dissection with incomplete Horner syndrome. Figure 1. A , T2-TIRM (turbo inversion recovery magnitude) dark fluid MRI, axial slices; this sequence shows the typical intramural hematoma in the left ICA (arrow). B , T1 TSE (turbo spin echo) with fat saturation, coronal slices; use of fat-saturation technique shows bright (met-hemoglobin containing) hematoma in the left ICA below the scull base. Extracranial and intracranial duplex sonography revealed a resistance flow profile in the dissected ICA indicating distal occlusion. Collateral circulation through the left posterior communicating artery maintained the blood flow in the left anterior and middle cerebral artery. Six days later a repeated ultrasound showed improving blood flow with only local flow accelerations in the distal extracranial portion of the dissected ICA. The patient was treated with aspirin 300 mg daily for 2 weeks followed by a dose reduction to 100 mg daily. During hospitalization, she remained clinically stable and was discharged home after 8 days. At …

Incomplete Horner's syndrome as a presenting sign of fourth ventricle ependymoma

Case reportThe case of 44-year-old male patient with palpebral ptosis and trigeminal neuralgia as presenting sign of fourth ventricle ependymoma is reported. After surgical treatment, the patient developed a residual paresis of the sixth cranial nerve. DiscussionHorner's syndrome occurs due to an alteration of the sympathetic innervations of the eye and adnexa. Some tumors may be the cause, in our case an ependymoma of the fourth ventricle, which onset exceptionally with blepharoptosis and involvement of the ophthalmic division of trigeminal nerve, due to the proximity of these nerve fibers at the brainstem.

Attempted reversible sympathetic ganglion block by an implantable neurostimulator

Primary palmar hyperhidrosis is a pathological condition of excessive perspiration of the hands of unknown aetiology. The only effective treatment for permanent cure is the ablation of the sympathetic ganglia supplying the hands. One of the sequelae is compensatory sweating, namely increased perspiration in other parts of the body. Its mechanism is unknown. In a small proportion of patients, it may attend devastating proportions. It has practically no remedy, and the degree of compensatory hyperhidrosis is unpredictable prior to sympathectomy. The purpose of the present study was to obtain a reversible sympathetic block which may disclose subjects prone to develop severe compensatory hyperhidrosis and unfit for permanent ganglionic ablation. In three dogs, an experimental electrode was implanted via a left thoracotomy on the stellate ganglion, connected to a stimulator. The stimulation was activated after recovery. The contralateral ganglion served as control. Effect of the stimulation was assessed by observing the development of Horner's syndrome, which includes the appearance of miosis, ptosis and enophthalmus. Reversal of the sympathetic block was expected when the neurostimulation was discontinued and assessed by the disappearance of these signs. Stimulation produced only a partial effect - an incomplete Horner's syndrome (miosis and sometime ptosis), which was not completely reversible after ceasing the stimulation. Although neurostimulation achieved a partial sympathetic block, the present method failed to obtain a completely reversible effect. However, these results may indicate that different nervous pathways moderate the various components of the Horner's triad. Concerning the creation of a reversible sympathectomy; other approaches must be sought after.

Incomplete Horner Syndrome: Report of a Case and Description of the Sympathetic Nervous System Anatomy Involved in Horner Syndrome

Horner syndrome, in which ptosis, miosis, and anhidrosis occur concomitantly, can arise from injury to the sympathetic nerve pathways anywhere from the brain to the end organs. Incomplete Horner syndrome lacks the sign of anhidrosis. We present a case of incomplete Horner syndrome caused by internal carotid artery dissection and provide a road map of the cervical sympathetic nerves involved in Horner syndrome to explain its etiology. We also discuss the imaging of and therapy for internal carotid artery dissections.

Johan Georg Ræder (1889–1959) and paratrigeminal sympathetic paresis

Johan Georg Raeder (1889-1959) was the most eminent Norwegian ophthalmologist in the early decades of the last century. Raeder made significant contributions to our current understanding of glaucoma. He is remembered for a syndrome he described, that of trigeminal nerve neuralgia and/or paresis and incomplete Horner's syndrome (oculopupillary sympathetic paresis). Here, Raeder's biography, scientific contributions, and a thorough review of his original report on paratrigeminal sympathetic paresis are presented. Raeder's syndrome may reflect a lesion of the middle cranial fossa, which involves oculopupillary sympathetic fibers that originate from the internal carotid artery plexus and travel with the trigeminal and oculomotor nerves.

Diagnose und Verlauf von Carotisdissektionen*

33 patients with angiographically confirmed dissection of the internal carotid artery (ICA) were followed prospectively. Cardinal symptoms were: 1) focal disturbances of the cerebral circulation (n = 28); 2) unilateral headache or neck pain (n = 20); 3) incomplete Horner's syndrome (n = 9). Neurological deficits without pain or sympathetic nerve damage developed in 11 patients. All patients had abnormal Doppler ultrasound findings over the ICA; in 22 there were markedly reduced flow velocities and retrograde flow components ("to- and- fro" phenomenon), typical of carotid artery dissection. During a mean observation time of 6.9 +/- 5.7 months serial Doppler ultrasound and angiographic examinations demonstrated recanalization in 73% after an average of 56 days. Angiographically different types (long segments in 13; pseudo-occlusions in 7; pseudoaneurysms in 5; and distal stenoses in 6; others in 2) are interpreted as expressions of different stages in the development of dissection up to complete recanalization.

Abducens Nerve Palsy and Ipsilateral Incomplete Horner Syndrome: A Significant Sign of Locating the Lesion in the Posterior Cavernous Sinus

Abducens Nerve Palsy and Ipsilateral Incomplete Horner Syndrome: A Significant Sign of Locating the Lesion in the Posterior Cavernous Sinus

Cervical and intracranial arterial dissection: review of the acute clinical presentation and imaging of 48 cases

Arterial dissections result from longitudinal tear of the vessel wall produced by an intramural haematoma. We have retrospectively review 48 consecutive patients with 53 arterial dissections diagnosed by cerebral angiography and/or magnetic resonance imaging. Arterial dissections were extracranial in 88% (carotid in 58% and vertebral in 30%) and intracranial in 12% of cases, with 19% of multiple dissections. Extracranial dissections presented with infarct (82%) (major 52%, multifocal 16%, focal 28% e watershed 4%), cervical pain and/or headache (38%) incomplete Horner syndrome (14%). The intracranial dissections presented with infarct, intracranial hypertension and hydrocephalus, subarachnoid hemorrhage and brain haematoma. Most common angiographic findings in the extracranial carotid dissections were stenosis with slow flow (66%), occlusion (34%) and dissecting aneurysm (7%). In the extracranial vertebral dissections the angiograms depicted stenosis with slow flow (82%), occlusion (18%) and dissecting aneurysm (18%). In the intracranial dissections stenosis and dissecting aneurysm were equally found. Extracranial arterial dissections have are an important cause of stroke in the younger population. Anti thrombotic drugs are used for the treatment of dissections presenting with infarct. Refractory extracranial dissections and intracranial dissection with haemorrhage presentation and/or dissecting aneurysms should be managed by endovascular treatment.

Raeder's syndrome.

GEORGE Raeder,1a Norwegian neurologist, in 1918 first described a disturbance of the oculopupillary fibers associated with an incomplete Horner syndrome. The patient had headache, vomiting, pain in the left trigeminal area, paresis of the left side of the palate, and ptosis, miosis, and hypotonia, on the left, without vasomotor or trophic disturbances. The patient died of pulmonary tuberculosis, and necropsy revealed a tumor, described as an endothelioma, between the internal carotid artery and the Gasserian ganglion. The cervical sympathetic trunk was carefully examined down to the third thoracic segment without any lesion being found. This case was of extreme interest, since it presented a sympathetic syndrome quite distinct in anatomical localization from the ordinary sympathetic syndrome produced by spinal lesions or lesions of the cervical sympathetic fibers. Raeder suggested, therefore, that lesions of the sympathetic fibers be classified as follows: In 1924 Raeder reported four more cases of