Oculosympathetic Palsy Research Articles

Traumatic pseudoaneurysm of the internal carotid artery presenting with oculosympathetic palsy

Blunt internal carotid artery (ICA) injury is rare but undiagnosed can have disastrous clinical consequences. To report a late presentation of blunt ICA injury in a young male following a road traffic accident. A 16-year-old male presented 11 days following a head injury with a unilateral Horner's syndrome. Imaging confirmed a pseudoaneurysm of the ICA. The patient was treated with anticoagulant therapy. Diagnosis of ICA injury requires a high index of suspicion and presentation with unusual neurological signs following blunt trauma to the head and neck requires prompt investigation.

Painful Oculosympathetic Palsy as the Sole Presentation of Spontaneous Dissection of the Distal Internal Carotid Artery

Painful Oculosympathetic Palsy as the Sole Presentation of Spontaneous Dissection of the Distal Internal Carotid Artery

Painful oculosympathetic palsy as the sole presentation of spontaneous dissection of the distal internal carotid artery

Spontaneous dissection of the carotid artery is an important differential diagnosis to consider in cases of early onset stroke. Its natural history is variable, ranging from a benign course to permanent disability or death. Dissection usually occurs in the cervical portion of the artery, rendering it amenable to surgical therapy. These issues are compounded if there is intrapetral extension, with associated mortality rates up to 75%. The authors describe such a case of spontaneous dissection and discuss imaging and therapy issues that result.

Cranial nerve palsy in spontaneous dissection of the extracranial internal carotid artery

Cranial nerve palsy was present in 23 of 190 consecutive adult patients (12%) with spontaneous dissection of the extracranial internal carotid artery. Ten patients (5.2%) had a syndrome of lower cranial nerve palsies (with invariable involvement of cranial nerve XII with or without additional involvement of cranial nerves XI, X, and IX), seven (3.7%) had palsy of cranial nerve V, and five (2.6%) had a syndrome of ocular motor palsies. Palsy of cranial nerve VIII and ischemic optic neuropathy occurred in one patient each. Three patients had dysgeusia without other cranial nerve involvement, presumably due to involvement of the chorda tympani nerve. Headache or face pain (often unilateral) was present in 83% of patients. Other associated manifestations were cerebral ischemic symptoms, bruits, or oculosympathetic palsy. In one patient, cranial nerve palsy was the only manifestation of internal carotid artery dissection, and in another patient, the disease presented only as a palsy of cranial nerve XII and oculosympathetic palsy. In six patients, a syndrome of hemicrania and ipsilateral cranial nerve palsy was the sole manifestation of internal carotid artery dissection. Cranial nerve palsy is not rare in internal carotid artery dissection. Compression or stretching of the nerve by the expanded artery may explain some but not all of the palsies. An alternative mechanism is likely interruption of the nutrient vessels supplying the nerve.

Noninvasive Investigation of Pericarotid Syndrome: Role of MR Angiography in the Diagnosis of Internal Carotid Dissection

A 52-year-old man presented with unilateral left periorbital and frontotemporal pain associated with a partial ipsilateral Horner's syndrome of the postganglionic type and representing a pericarotid syndrome. MRI demonstrated a perivascular subacute hematoma at the level of the cervical portion of the left internal carotid artery with a markedly reduced flow-void signal. MR angiography confirmed the narrowed lumen of the dissected cervical internal carotid artery. There was also a right-sided precavernous carotid aneurysm. Three months later the left-sided pain had subsided, with complete resolution of the hematoma and incomplete restoration of the left carotid lumen seen on MR angiography. Dissection of the carotid wall may cause the oculosympathetic paralysis by producing a lesion of the superior cervical ganglion, the internal carotid nerve, or the perivascular sympathetic plexus. Whereas in pericarotid syndrome the most common cause is cervical carotid dissection, Raeder's syndrome additionally involving parasellar cranial nerves, may be caused by any paracavernous/cavernous lesion, including neoplasms and intracranial carotid aneurysms. The clinical distinction is useful to determine the appropriate diagnostic investigation, in view of the different pathoanatomical localization and different disease spectrum. As demonstrated in the present case, the combination of MRI and MR angiography is a reliable noninvasive tool to investigate the differential diagnosis of pericarotid syndrome, accurately depicting occlusive, stenotic or aneurysmal lesions of the carotid artery. We suggest that intraarterial angiography is no longer necessary.

Spontaneous internal carotid artery dissection: early diagnosis and management in 44 patients.

First symptoms and initial clinical, ultrasonographic and neuroradiological findings ascertained a mean of 5.6 days (SD = 5.6 days), 7.7 days (7.0), and 11.2 days (8.0) after symptom onset were analysed in 44 patients who suffered a spontaneous internal carotid artery dissection (ICD) verified by magnetic resonance imaging, angiography, or both. Common symptoms signalling dissection were unilateral headache in 68%, transient ischaemic attack in 20%, and cerebral infarction in 9%. Severe pain preceded cerebral ischaemia by more than 3 days in 60% of those patients who eventually suffered a stroke. However, only 2 were admitted because of pain alone and 33 for evolving neurological deficits. During the first month, ipsilateral severe headache occurred in 89%, neck pain in 36%, ipsilateral cerebral ischaemia in 82%, ocular ischaemia in 16%, oculosympathetic palsy in 48%, and cranial nerve palsy in 5%. Recent "trivial" head or neck trauma was elicited in 41%. Doppler and duplex sonography confirmed the clinical suspicion of ICD in 91.5% and in 96% of those with a significant stenosis or occlusion. MRI demonstrated a thickened vessel wall in all 33 imaged carotid dissections and a mural haematoma in 30. None of the 32 patients who received anticoagulant treatment subsequently deteriorated. Monitoring anticoagulant treatment with ultrasonographic follow-up studies demonstrated recanalization in 70% and persistent occlusion in 30%. The results demonstrate that familiarity with the initial symptoms, especially headache, and performance of an ultrasonographic study without delay are the cornerstones of an early diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Cervicocranial Arterial Dissection

Abstract Dissection of the cervicocranial arteries is becoming more frequently recognized as a cause of neurological disorders. Typical clinical features seen with dissection include unilateral headache, oculosympathetic palsy, amaurosis fugax, and symptoms of focal brain ischemia. The diagnosis of carotid or intracranial dissection is usually best confirmed by angiography, although magnetic resonance imaging and computed tomography have been shown to visualize intimal dissection. The prognosis in cases of spontaneous dissection is generally benign unless the initial manifestation involves infarction with substantial deficit. The best approach to treatment appears to be the administration of the anticoagulant, heparin, followed by warfarin or antiplatelet therapy. Surgical intervention is reserved for cases of progressive or recurrent ischemic complication that occurs despite the administration of adequate doses of anticoagulants. (Neurosurgery 29:89-96, 1991)

Cervicocranial arterial dissection

Dissection of the cervicocranial arteries is becoming more frequently recognized as a cause of neurological disorders. Typical clinical features seen with dissection include unilateral headache, oculosympathetic palsy, amaurosis fugax, and symptoms of focal brain ischemia. The diagnosis of carotid or intracranial dissection is usually best confirmed by angiography, although magnetic resonance imaging and computed tomography have been shown to visualize intimal dissection. The prognosis in cases of spontaneous dissection is generally benign unless the initial manifestation involves infarction with substantial deficit. The best approach to treatment appears to be the administration of the anticoagulant, heparin, followed by warfarin or antiplatelet therapy. Surgical intervention is reserved for cases of progressive or recurrent ischemic complication that occurs despite the administration of adequate doses of anticoagulants.

Protrusion of the first thoracic disk

A case of lateral prolapse of the T-1/T-2 intervertebral disk is presented. The patient complained of pain radiating down the medial aspect of the forearm into the little and ring fingers. This was associated with a subjective sensory loss in the same distribution, intact reflexes, and no long tract signs. Oculosympathetic paralysis was not present. Twelve cases have been mentioned in the literature, only eight of which contain details of the neurological findings. The varied findings in these cases are also reviewed, and it is noted that unless radiological examination includes the upper thoracic spine in cases of brachial neuralgia, these lesions will be missed.

Traumatic dissections of the extracranial internal carotid artery.

Traumatic dissections of the extracranial internal carotid artery (ICA) in 18 patients aged 19 to 55 years were studied. All had suffered blunt head or neck injury of marked or moderate severity; motor-vehicle accidents were the leading cause of the injury. Delayed focal cerebral ischemic symptoms were the most common presenting symptoms. Less commonly noted was focal unilateral headache associated with oculosympathetic paresis or bruit. Following a head injury, the abrupt onset of focal cerebral symptoms after a lucid interval should raise the suspicion of arterial injury, particularly when computerized tomography fails to show abnormalities that would explain the evolving neurological deficits on the basis of direct trauma to the brain. Unilateral headaches, oculosympathetic palsy, and bruits also help in establishing the diagnosis. Focal cerebral ischemic symptoms may develop months or years after the initial trauma. These delayed symptoms are caused by embolization from a thrombus within a residual dissecting aneurysm. Common angiographic findings, in decreasing order of frequency, are: aneurysm, stenosis of the lumen, occlusion, intimal flap, distal branch occlusion (embolization), and slow ICA-to-middle cerebral artery flow. Although two patients died as the result of massive cerebral infarction and edema and some were left with severe neurological deficits, most made a good recovery. Residual dissecting aneurysms and occlusion seem to occur more frequently with traumatic dissections than with spontaneous dissections of the extracranial ICA.

Painful Horner's Syndrome Due to Spontaneous Carotid Artery Dissection

Spontaneous dissection of the internal carotid artery as a cause of Horner's syndrome has only been recognized in recent years. The authors describe three patients with this condition. Associated symptoms included ipsilateral orbital and frontal headache (3 patients), neck and facial pain (2), amaurosis fugax (1), and dysgeusia (1). The symptoms resolved in all patients within three months, yet oculosympathetic paralysis has persisted. Diagnosis of carotid dissection required cerebral arteriography, and the angiographic features are presented. Patients were treated with platelet antiaggregants, and they have remained neurologically stable during follow-up (mean, 12 months; range, 10–14 months).

Topographic analysis of Horner's syndrome.

Horner's syndrome or oculosympathetic paralysis is not an uncommon finding in patients with head and neck neoplasms. While in most cases the syndrome is easily established at the bedside, it can be confirmed and topographically defined as a central, preganglionic, or postganglionic lesion through sequential pharmacologic testing. The importance of such localization lies in differentiating neoplasia vs. a benign condition as the cause of the syndrome. Such variants as congenital Horner's, an alternating Horner's, and a pseudo-Horner's syndrome are discussed in regard to their differential features.

Pseudo-Horner's syndrome.

• Eighteen patients who were studied for Horner's syndrome were found to have ipsilateral ptosis and miosis not due to oculosympathetic paralysis. A systematic approach to the diagnosis of Horner's syndrome should include pharmacologic pupillary testing with topically applied cocaine.

Oculosympathetic Paresis

Of 100 consecutive, adult, hospitalized inpatients with acquired unilateral oculosympathetic palsy, in 63 the central neuron was involved-usually due to strokes; in 21, tumor or trauma affected the preganglionic neuron; and in 13, postganglionic damage was sustained from a variety of causes. The preponderance of first neuron involvement by stroke is in part a reflection of patient sampling, but emphasizes the fact that central causes of Horner's syndrome are common.

Spontaneous Dissection of Cervico-Cerebral Arteries

Sixteen cases of spontaneous dissection of the cervical internal carotid artery (6 verified) are described. The mean age was 45 years. The clinical picture varied from simply headache and a bruit to hemiplegia and aphasia. Eleven patients had transient ischemic attacks. Headache, facial pain, a subjective bruit, oculo-sympathetic palsy and transient monocular blindness were present in various combinations in two-thirds of cases and their presence suggested the correct diagnosis. Examples of suspected dissection of the intracranial internal carotid, middle cerebral, posterior cerebral and extracranial vertebral arteries are also presented. Spontaneous dissection is more common than the literature indicates.

EVIDENCE FOR AUTOREGULATION IN HUMAN RETINAL CIRCULATION

The pressure gradient across the walls of retinal arteries can be decreased by raising intraocular tension. The calibre of retinal arteries was measured in patients with normal vascular innervation and in patients with oculosympathetic paralysis by a photographic method before and after raising intraocular tension by pressing lightly on the globe. A significant increase in calibre of about 16% was found in arteries but not in veins when the intraocular tension was raised, both in normal patients and in those with sympathetic paralysis. The change was present within 2 minutes of alteration in ocular tension. This reaction is likely to be a local myogenic reflex, independent of innervation and concerned with the regulation of blood-flow.

Otitis media and complications 1961.

The past year has been noteworthy for original ideas on cholesteatoma and a considerable number of articles on intracranial complications of otitis media. Acute Otitis Media Hoefnagel and Joseph (Boston) 1 reported an unusual finding in 5 children with acute otitis media: oculosympathetic paralysis. The symptoms were drooping of the upper eyelid and narrowing of the pupil on the side of the otitis media. This resembles Horner's syndrome, but the absence of sweating of the forehead and face on the affected side, sometimes seen in Horner's syndrome, was not seen. A few reports of this condition have been made before. They explain the findings by a diagram that shows sympathetic nerve fibers coming up from the superior cervical ganglion along the plexus around the internal carotid artery, across the floor of the middle ear (where the paralysis may occur) and out along the vidian nerve to the ophthalmic nerve. The

Oculosympathetic paralysis in otitis media.

OCULOSYMPATHETIC paralysis is a paralysis caused by damage to the sympathetic nerve fibers that innervate the smooth muscles of eye and orbit; it manifests itself clinically by a slight droop of the upper eyelid and a narrowing of the homo-lateral pupil. The paralysis differs from a complete Horner syndrome because anhidrosis of face and forehead, sometimes present in the latter, is absent in oculosympathetic paralysis. Although this type of paralysis has received most attention as an accompanying sign of unilateral vascular headaches in adults1 some clinical reports2 3 4 5 have called attention to its presence after surgery of the middle ear or . . .