Horner Syndrome
Abducens Nerve Diseases
Mydriasis
Isolated Horner's syndrome and syringomyelia. (1/97)
Although syringomyelia has been associated with Horner's syndrome, it is typically associated with other neurological findings such as upper limb weakness or numbness. A patient is described who had an isolated Horner's syndrome as the only manifestation of syringomyelia. A 76 year old woman was discovered to have right upper lid ptosis and right pupillary miosis. Neurological examination was unremarkable, and pharmacological testing was consistent with localisation of the lesion to a first or second order sympathetic neuron. Neuroimaging disclosed a Chiari I malformation with a syrinx extending to the C2 to C4 level. An isolated Horner's syndrome may be the presenting manifestation of syringomyelia. (+info)Course and distribution of facial corticobulbar tract fibres in the lower brain stem. (2/97)
The course and distribution of the facial corticobulbar tract (CBT) was examined by correlating MRI of brain stem lesions with neurological symptoms and signs including central (C-FP) or peripheral facial paresis (P-FP) in 70 patients with localised infarction of the lower brain stem. C-FP occurred more often in patients with lesions of the lower pons or upper medulla of the ventromedial brain stem. Some patients with dorsolateral infarcts of the upper medulla to the lower pons showed C-FP, mostly on the lesion side. P-FP on the side of the lesion was also seen in patients with dorsolateral involvement of the lower pons. Patients with ventromedial infarction of the brain stem showed paresis of extremities contralateral to the lesion. Specific neurological symptoms and signs such as dysphagia, vertigo, nystagmus, Horner's syndrome, ipsilateral cerebellar ataxia, and contralateral superficial sensory impairment were seen in patients with dorsolateral infarcts of the brain stem. It is hypothesised that the facial CBT descends at the ventromedial lower pons, near the corticospinal tract, mainly to the level of the upper medulla, where the fibres then decussate and ascend in the dorsolateral medulla to synapse in the contralateral facial nucleus. (+info)First rib fracture: a hallmark of severe trauma. (3/97)
First rib fractures occurred in 55 patients. This injury is a harbinger of major trauma with 35 patients suffering a major chest injury, and abdominal and cardiac injuries occurring in 18 and eight patients respectively. The mortality associated with this injury was high (36.3%). Neurologic lesions accounted for the majority of deaths, however, unrecognized abdominal injuries and pulmonary complications were significant causes of mortality. Brachial plexus injury (5) and Horner's syndrome (3) occurred in survivors. Three patients had an associated injury of the subclavian artery, and the importance of this association is stressed. One late-developing post-traumatic thoracic outlet syndrome occurred. A fracture of the first rib is a hallmark of severe trauma; its presence should alert the clinician to: 1) generalized massive trauma with abdominal, chest, and cardiac injuries; 2) local injury to the subclavian artery and brachial plexus and; 3) necessity of long-term followup for late-developing sequelae. (+info)A case of Brown-Sequard syndrome with associated Horner's syndrome after blunt injury to the cervical spine. (4/97)
A 26 year old motorcyclist was received by the trauma team in our accident and emergency department after a head on collision with a motor vehicle. He had been correctly immobilised and his primary survey was essentially normal. He was alert and orientated with a Glasgow Coma score of 15 and had no symptoms or signs of spinal injury. His cervical spine radiography was also normal. Neurological examination however, revealed anisocoria, his left pupil being smaller than his right, and a Brown-Sequard syndrome, with a sensory level at C6. Immobilisation was maintained and he was transferred to the regional neurosurgical centre where magnetic resonance imaging revealed a contusion of the left half of the spinal cord adjacent to the 6th cervical vertebrae. Computed tomography revealed no bony injury but spinal column instability was demonstrated after flexion-extension spinal views and he underwent surgery to fuse his spine at the C5-C6 level. This report highlights the necessity to observe strict ATLS guidelines. This must include a thorough examination of the central and peripheral nervous system where spinal injury is suspected, even in the absence of radiographic abnormality and neck pain. This article also presents the unusual phenomena of Brown-Sequard syndrome and unilateral Horner's syndrome after blunt traumatic injury to the cervical spine. (+info)Isolated abducens nerve paresis associated with incomplete Horner's syndrome caused by petrous apex fracture--case report and anatomical study. (5/97)
A 17-year-old male presented with a wound on the right temporal region, oozing hemorrhagic necrotic brain tissue and cerebrospinal fluid, following a fall. Computed tomography showed temporoparietal and petrous apex fractures on the right. Neurological examination revealed abducens nerve paresis, ptosis, and myosis on the right side. The patient was treated surgically for the removal of the free bony fragments at the fracture site and to close the dural tear. The abducens nerve paresis, ptosis, and myosis persisted at the 3rd monthly postoperative follow-up examination. The anatomy of the abducens nerve at the petroclival region was studied in four cadaveric heads. Two silicone-injected heads were used for microsurgical dissections and two for histological sections. The abducens nerve has three different angulations in the petroclival region, located at the dural entrance porus, the petrous apex, and the lateral wall of the cavernous segment of the internal carotid artery. The abducens nerve had fine anastomoses with the trigeminal nerve and the periarterial sympathetic plexus. There were fibrous connections extending inside the venous space of the petroclival area. The abducens nerve seems to be vulnerable to damage in the petroclival region, either directly by trauma to its dural porus and petrous apex or indirectly by stretching of the nerve through the nervous and/or fibrous connections. Concurrent functional loss of the abducens nerve and the periarterial sympathetic plexus clinically manifested as incomplete Horner's syndrome in our patient. (+info)Agenesis of the internal carotid artery associated with aortic arch anomaly in a patient with congenital Horner's syndrome. (6/97)
We report a rare case of agenesis of the left internal carotid artery (ICA) and an aortic arch anomaly that presented with ipsilateral congenital Horner's syndrome. Digital subtraction angiography revealed left ICA agenesis shortly after its origin and anastomosis between the left maxillary artery and the supraclinoid segment of the left ICA. Aortography of the aortic arch revealed the right subclavian artery arising as the first branch of a left aortic arch, followed by a bicarotid trunk and a left subclavian artery. High resolution CT of the skull base revealed the absence of the left carotid channel, consistent with congenital agenesis of the ICA. (+info)Trigeminal and polyradiculoneuritis in a dog presenting with masticatory muscle atrophy and Horner's syndrome. (7/97)
A 9-year-old, spayed female, Airedale Terrier was euthanatized and necropsied after a progressive clinical course that included Horner's syndrome of the left eye and unilateral atrophy of the masticatory muscles. Although gross lesions were limited, a polyradiculoneuritis and ganglionitis that was most severe in the trigeminal nerves and ganglia were confirmed histologically. The inflammatory infiltrate consisted predominantly of macrophages and B and T lymphocytes that were phenotypically confirmed by immunostaining. Horner's syndrome was the result of damage to postganglionic sympathetic fibers that were incorporated in segments of the inflamed trigeminal nerve and its ophthalmic branch. Histologically, the character and distribution of the inflammation was similar to previously described syndromes of suspected immune-mediated etiology in humans and animals. (+info)Artemin is a vascular-derived neurotropic factor for developing sympathetic neurons. (8/97)
Artemin (ARTN) is a member of the GDNF family of ligands and signals through the Ret/GFRalpha3 receptor complex. Characterization of ARTN- and GFRalpha3-deficient mice revealed similar abnormalities in the migration and axonal projection pattern of the entire sympathetic nervous system. This resulted in abnormal innervation of target tissues and consequent cell death due to deficiencies of target-derived neurotrophic support. ARTN is expressed along blood vessels and in cells nearby to sympathetic axonal projections. In the developing vasculature, ARTN is expressed in smooth muscle cells of the vessels, and it acts as a guidance factor that encourages sympathetic fibers to follow blood vessels as they project toward their final target tissues. The chemoattractive properties of ARTN were confirmed by the demonstration that sympathetic neuroblasts migrate and project axons toward ARTN-soaked beads implanted into mouse embryos. (+info)Horner syndrome, also known as Horner's syndrome or oculosympathetic palsy, is a neurological disorder characterized by the interruption of sympathetic nerve pathways that innervate the head and neck, leading to a constellation of signs affecting the eye and face on one side of the body.
The classic triad of symptoms includes:
1. Ptosis (drooping) of the upper eyelid: This is due to the weakness or paralysis of the levator palpebrae superioris muscle, which is responsible for elevating the eyelid.
2. Miosis (pupillary constriction): The affected pupil becomes smaller in size compared to the other side, and it may not react as robustly to light.
3. Anhydrosis (decreased sweating): There is reduced or absent sweating on the ipsilateral (same side) of the face, particularly around the forehead and upper eyelid.
Horner syndrome can be caused by various underlying conditions, such as brainstem stroke, tumors, trauma, or certain medical disorders affecting the sympathetic nervous system. The diagnosis typically involves a thorough clinical examination, pharmacological testing, and sometimes imaging studies to identify the underlying cause. Treatment is directed towards managing the underlying condition responsible for Horner syndrome.
The abducens nerve, also known as the sixth cranial nerve, is responsible for controlling the lateral rectus muscle of the eye, which enables the eye to move outward. Abducens nerve diseases refer to conditions that affect this nerve and can result in various symptoms, primarily affecting eye movement.
Here are some medical definitions related to abducens nerve diseases:
1. Abducens Nerve Palsy: A condition characterized by weakness or paralysis of the abducens nerve, causing difficulty in moving the affected eye outward. This results in double vision (diplopia), especially when gazing towards the side of the weakened nerve. Abducens nerve palsy can be congenital, acquired, or caused by various factors such as trauma, tumors, aneurysms, infections, or diseases like diabetes and multiple sclerosis.
2. Sixth Nerve Palsy: Another term for abducens nerve palsy, referring to the weakness or paralysis of the sixth cranial nerve.
3. Internuclear Ophthalmoplegia (INO): A neurological condition affecting eye movement, often caused by a lesion in the medial longitudinal fasciculus (MLF), a bundle of nerve fibers that connects the abducens nucleus with the oculomotor nucleus. INO results in impaired adduction (inward movement) of the eye on the side of the lesion and nystagmus (involuntary eye movements) of the abducting eye on the opposite side when attempting to look towards the side of the lesion.
4. One-and-a-Half Syndrome: A rare neurological condition characterized by a combination of INO and internuclear ophthalmoplegia with horizontal gaze palsy on the same side, caused by damage to both the abducens nerve and the paramedian pontine reticular formation (PPRF). This results in limited or no ability to move the eyes towards the side of the lesion and impaired adduction of the eye on the opposite side.
5. Brainstem Encephalitis: Inflammation of the brainstem, which can affect the abducens nerve and other cranial nerves, leading to various neurological symptoms such as diplopia (double vision), ataxia (loss of balance and coordination), and facial weakness. Brainstem encephalitis can be caused by infectious agents, autoimmune disorders, or paraneoplastic syndromes.
6. Multiple Sclerosis (MS): An autoimmune disorder characterized by inflammation and demyelination of the central nervous system, including the brainstem and optic nerves. MS can cause various neurological symptoms, such as diplopia, nystagmus, and INO, due to damage to the abducens nerve and other cranial nerves.
7. Wernicke's Encephalopathy: A neurological disorder caused by thiamine (vitamin B1) deficiency, often seen in alcoholics or individuals with malnutrition. Wernicke's encephalopathy can affect the brainstem and cause various symptoms such as diplopia, ataxia, confusion, and oculomotor abnormalities.
8. Pontine Glioma: A rare type of brain tumor that arises from the glial cells in the pons (a part of the brainstem). Pontine gliomas can cause various neurological symptoms such as diplopia, facial weakness, and difficulty swallowing due to their location in the brainstem.
9. Brainstem Cavernous Malformation: A benign vascular lesion that arises from the small blood vessels in the brainstem. Brainstem cavernous malformations can cause various neurological symptoms such as diplopia, ataxia, and facial weakness due to their location in the brainstem.
10. Pituitary Adenoma: A benign tumor that arises from the pituitary gland, located at the base of the brain. Large pituitary adenomas can compress the optic nerves and cause various visual symptoms such as diplopia, visual field defects, and decreased vision.
11. Craniopharyngioma: A benign tumor that arises from the remnants of the Rathke's pouch, a structure that gives rise to the anterior pituitary gland. Craniopharyngiomas can cause various neurological and endocrine symptoms such as diplopia, visual field defects, headaches, and hormonal imbalances due to their location near the optic nerves and pituitary gland.
12. Meningioma: A benign tumor that arises from the meninges, the protective covering of the brain and spinal cord. Meningiomas can cause various neurological symptoms such as diplopia, headaches, and seizures depending on their location in the brain or spinal cord.
13. Chordoma: A rare type of malignant tumor that arises from the remnants of the notochord, a structure that gives rise to the spine during embryonic development. Chordomas can cause various neurological and endocrine symptoms such as diplopia, visual field defects, headaches, and hormonal imbalances due to their location near the brainstem and spinal cord.
14. Metastatic Brain Tumors: Malignant tumors that spread from other parts of the body to the brain. Metastatic brain tumors can cause various neurological symptoms such as diplopia, headaches, seizures, and cognitive impairment depending on their location in the brain.
15. Other Rare Brain Tumors: There are many other rare types of brain tumors that can cause diplopia or other neurological symptoms, including gliomas, ependymomas, pineal region tumors, and others. These tumors require specialized diagnosis and treatment by neuro-oncologists and neurosurgeons with expertise in these rare conditions.
In summary, diplopia can be caused by various brain tumors, including pituitary adenomas, meningiomas, chordomas, metastatic brain tumors, and other rare types of tumors. It is important to seek medical attention promptly if you experience diplopia or other neurological symptoms, as early diagnosis and treatment can improve outcomes and quality of life.
Mydriasis is a medical term that refers to the dilation or enlargement of the pupil, which is the black circular opening in the center of the iris (the colored part) of the eye. The pupil normally adjusts its size in response to changes in light levels and emotional state. In mydriasis, the pupil becomes widely dilated and less responsive to light. This can occur naturally due to factors such as strong emotions, fear, or physical exertion, but it can also be caused by certain medications, eye drops, or medical conditions like brain injuries or neurological disorders. It is important to note that mydriasis can affect one or both eyes and may have different clinical significance depending on the context.
A carotid artery, internal, dissection is a medical condition that affects the internal carotid artery, which is a major blood vessel in the neck that supplies oxygenated blood to the brain. In this condition, there is a separation (dissection) of the layers of the artery wall, causing blood to accumulate in the space between the layers. This can lead to narrowing or blockage of the artery, reducing blood flow to the brain and increasing the risk of stroke. Internal carotid artery dissection can be caused by trauma, high blood pressure, connective tissue disorders, or spontaneously. Symptoms may include neck pain, headache, facial pain, visual disturbances, weakness or numbness in the arms or legs, difficulty speaking or understanding speech, and dizziness or loss of balance.